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PubMed · 8924554

[Microscopic polyarteritis].

C de Ancos Aracil·J L Rebollar Mesa
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Abstract

Microscopic polyarteritis is a type of vasculitis that shows similar characteristics to other illnesses from the same group. This group presents a common clinical fact: a rapidly progressive glomerulonephritis. We specially point out among this group of illnesses the Wegener granulomatosis. The anti-neutrophil cytoplasmic antibodies is important for two different reasons. The fact that sometimes they have allowed to make differential diagnosis and that they represents so far the only serologic marking of such vasculitis. The ANCA antimieloperoxidasa (p-ANCA) can be found in a greater level in microscopic poliarteritis as well as the antiproteinasa-3 (c-ANCA) in the Wegener granulomatosis. The current revision tries to clarify the differential diagnosis of the microscopic poliarteritis, which nowadays is still quite vague. This lack can be compensated thanks to the fact that the therapeutic treatment of this group of illnesses is very similar.

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Antibodies, Antineutrophil CytoplasmicDisease ProgressionGlomerulonephritisGranulomatosis with PolyangiitisHumansPolyarteritis NodosaSyndromeEnglish AbstractJournal ArticleReview

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C de Ancos Aracil, J L Rebollar Mesa. 1995. [Microscopic polyarteritis].. https://pubmed.ncbi.nlm.nih.gov/8924554/

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Dissociation between high anti-PR3 titers (c-ANCA) and the clinical course of disease in a case of Wegener granulomatosis.

In May 1984 a 58-year-old woman presented with a broad spectrum of clinical symptoms including malaise, arthralgia, hemoptysis and dyspnea, proteinuria and hematuria and a vasculitic necrotizing rash. Bronchial biopsies revealed subglottic granulomatous lesions and renal biopsies showed necrosis, extracapillary proliferation and crest formation, confirming the diagnosis of Wegener granulomatosis. Positive c-ANCA and anti-proteinase 3 subfraction (anti-PR3) titers were first analysed in 1991. Clinical remission was achieved by standard immunosuppressive therapy and renal function was stabilised. Several minor relapses were treated with pulsed intravenous cyclophosphamide but the symptoms could not be completely controlled. Eight years after the onset of disease, a dramatic increase in anti-PR3 titers was observed (34438 U/ml, normal range < 10, ELISA), followed 3 months later by a clinically apparent relapse. Immunosuppressive therapy was reinstituted without clinical improvement. At this point plasmapheresis resulted in an amelioration of clinical symptoms as well as a reduction in anti-PR3 titers. Concomitant immunosuppressive therapy was administered with oral corticosteroids. Forty days later anti-PR3 titers increased, reaching 75000 U/ml twelve months later, however this time without associated clinical symptoms. During the following months the patient had a further transient deterioration of pulmonary and renal function due to secondary bacterial infection which was successfully treated with antibiotics. A nephritic sediment was not present during these episodes. Curiously, the anti-PR3 titers have remained excessively elevated for the last three years.

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